BCL-2 EXPRESSING T-LYMPHOCYTES IN MULTIPLE-SCLEROSIS LESIONS

Citation
Uk. Zettl et al., BCL-2 EXPRESSING T-LYMPHOCYTES IN MULTIPLE-SCLEROSIS LESIONS, Neuropathology and applied neurobiology, 24(3), 1998, pp. 202-208
Citations number
39
Categorie Soggetti
Neurosciences,"Clinical Neurology",Pathology
ISSN journal
03051846
Volume
24
Issue
3
Year of publication
1998
Pages
202 - 208
Database
ISI
SICI code
0305-1846(1998)24:3<202:BETIML>2.0.ZU;2-9
Abstract
Multiple sclerosis (MS) is a chronic inflammatory disease of the centr al nervous system. T lymphocytes play a major role in the pathogenesis of the disease. The exact mechanisms by which the inflammation is reg ulated in MS have not yet been defined. Studies in animal models of MS suggest that apoptosis of T cells is the main factor terminating infl ammation. The process of apoptosis itself is regulated by a range of p ro- and anti-apoptotic proteins. The bcl-2 gene family is an important member of these proteins. The present study investigated the expressi on of the anti-apoptotic protein bcl-2 in 11 chronic MS cases includin g five relapsing-remitting and six chronic progressive MS patients. A total of 35 lesions containing all stages of demyelinating activity we re studied. The number of CD3-positive T cells and the absolute and re lative numbers of T cells expressing bcl-2 were determined by double i mmunocytochemistry. Bcl-2 is expressed by T lymphocytes in MS plaques. Patients with chronic progressive MS have a higher proportion of bcl- 2 expressing T cells than patients with relapsing remitting disease. H ighest numbers of bcl-2-positive T lymphocytes were found in remyelina ting and demyelinated lesions, whereas active demyelinating lesions re vealed lower numbers. These data indicate that cell-death-related prot eins such as the anti-apoptotic protein bcl-2 are expressed in MS lesi ons and that they might have important effects on the regulation of el imination or persistence of inflammatory cells in the central nervous system.